Report on the monitoring and testing of ruminants for the presence of transmissible spongiform encephalopathies (TSEs) in the EU in 2007 (2009)
Directorate E — Safety of the food chain E2 — Food Hygiene, Alert System and Training
1. Summary In 2007, a total of 9 711 123 bovine, 828 644 ovine and 277 196 caprine animals were tested in the EU 27 in the framework of the TSE monitoring programmes. 174 bovine, 2 253 ovine and 1272 caprine animals turned out positive. 1 445 280 risk bovine animals and 8 262 517 healthy animals slaughtered for human consumption were tested by rapid tests. 1 860 bovine animals were tested in the framework of passive surveillance (animals reported as official BSE suspects). In addition, 1 466 animals were tested in the framework of culling of animals with an epidemiological connection to a BSE case. 91 % of positive cases were detected by the active monitoring (testing of risk animals, healthy slaughtered and culled cattle) and 9 % were detected by passive surveillance. In 2007, no BSE case was found in Belgium, Bulgaria, Denmark, Estonia, Greece, Cyprus, Latvia, Lithuania, Luxembourg, Malta, Romania, Finland and Sweden. The number of BSE cases and the overall prevalence in tested animals decreased by respectively 46 % and 41 % in 2007 compared to 2006. 826 730 ovine animals were tested by active monitoring, while 1 914 were animals reported as official TSE suspects and therefore subjected to laboratory examination. In caprine animals, the numbers of tests in the respective groups were 276 040 (active monitoring) and 1 156 (TSE suspects). Some 987 and 112 TSE cases in respectively sheep and goats confirmed in 2007 were subjected to discriminatory testing. None of them have been confirmed to be BSE. In addition, in the framework of a survey for chronic wasting disease (CWD) in cervids, as required by Commission Decision 2007/182/EC, 10 843 animals were tested between 2006 and 2007 hunting seasons. None of them turned out positive. All Member States submitted information on the TSE testing of bovine, ovine and caprine animals. In addition to the Member States, Norway also submitted information on their TSE testing programmes.
see full text ;
NOW, compare to USA MAD COW TESTING, or the lack of $$$ ;
USDA to cut back BSE testing program Jul 20, 2006 (CIDRAP News) – The US government's expanded testing program for bovine spongiform encephalopathy (BSE) will be cut back soon, having shown that the nation has "no significant BSE problem," Agriculture Secretary Mike Johanns said today.
About 759,000 cattle, or more than 1,000 cattle per day, have been tested since the US Department of Agriculture (USDA) expanded BSE surveillance in June 2004, Johanns said at a news conference. Two cases were found during that time, in addition to the first US case discovered in 2003.
Starting as early as late August, testing will be reduced to about 40,000 cattle a year, or about 110 a week, Johanns announced. The reduced testing program—similar to what was done before the expansion—will cost about $8 million a year, versus about $52 million a year currently, he said.
To the suggestion that the current level of testing should continue indefinitely, Johanns said, "There simply is no scientific justification for doing so. . . . The reality is this: there is no significant BSE problem in the United States. And after all this surveillance I am able to say there never was. We've proved that with our enhanced surveillance."
Johanns said that testing 40,000 cattle a year is 10 times as many as recommended in the science-based guidelines of the World Organization for Animal Health (OIE). The USDA will continue to test cattle from high-risk populations and from a variety of places around the country, he said.
"To put it simply, we've accomplished our enhanced surveillance goals, and it's time to move forward with a level of surveillance that corresponds to the very low level of BSE in this country," he added. In a news release, he stated that the reduced testing program "will maintain our ability to detect BSE, [and] provide assurance that our interlocking safeguards are successfully preventing BSE."
The testing program was expanded in response to the first BSE case in 2003, with the aim of determining the disease's prevalence. The government originally proposed to test about 275,000 cattle over 12 to 18 months, but the program now has lasted more than 25 months.
The plan to reduce testing comes as Japan prepares to resume importing US beef, long banned because of BSE worries, and as the USDA tries to reopen South Korea and China to American beef. Japan has been inspecting US beef processing plants this month and, if the results are satisfactory, is expected to resume imports of beef from cattle younger than 20 months.
In response to questions, Johanns said the USDA told the nation's trading partners about the testing cutback in advance. He also said it would have been "enormously disingenuous, if not downright dishonest" if the USDA had waited until the foreign markets reopened and then reduced the testing program.
Johanns stressed that the testing program is not a food safety program but rather a way to assess the prevalence of BSE. The key to protecting food safety is removing the specified risk materials (SRM)—cattle parts such as the brain and spinal cord, which are likely to carry the BSE agent if an animal is infected, he said. Removal of SRM from carcasses of cattle older than 30 months has been required since early 2004.
Citing an analysis of the US surveillance program released in April, Johanns said, "Experts believe that in an adult cattle population of 42 million we might find four to seven animals with BSE." With BSE that rare and with the SRM ban in place, the risk of BSE-contaminated beef getting into the food supply is "virtually nonexistent."
Also at the news conference, Dr. Ron DeHaven, head of the USDA Animal and Plant Health Inspection Service, said the USDA is considering relaxing restrictions on imports of live Canadian cattle. Canada recently identified its sixth BSE case.
Because of BSE concerns, the only live Canadian cattle allowed into the United States are those destined for slaughter before reaching the age of 30 months. In response to a question, DeHaven said the USDA is considering allowing older cattle to be imported, because the Canadian system for preventing BSE "mirrors what we have in the US."
But he also said the USDA will consider any findings about Canada's latest BSE case before making any changes in the import rules. The latest case was in a 4-year-old cow, born years after a ban on putting recycled cattle protein into cattle feed took effect in 1997.
DeHaven also commented on recent reports that the two latest US BSE cases involved a different "strain" of prion protein from that seen in the first case and in European cases.
"Both the Alabama and the Texas cows had a slightly different prion" with a higher molecular weight than in previous cases, he said. He added that researchers are working to find out what that means.
"From the regulatory standpoint we're considering those to be two cases of BSE. But we feel very comfortable that our existing program provides the appropriate level of protection," regardless of the type of prion involved, DeHaven said.
Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program
An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.
4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half
full text ;
USDA: In 9,200 cases only one type of test could be used
WASHINGTON (AP)--The U.S. Department of Agriculture acknowledged Aug. 17 that its testing options for bovine spongiform encephalopathy were limited in 9,200 cases despite its effort to expand surveillance throughout the U.S. herd.
In those cases, only one type of test was used--one that failed to detect the disease in an infected Texas cow.
The department posted the information on its website because of an inquiry from The Associated Press.
Conducted over the past 14 months, the tests have not been included in the department's running tally of BSE tests since last summer. That total reached 439,126 on Aug. 17.
"There's no secret program," the department's chief veterinarian, John Clifford, said in an interview. "There has been no hiding, I can assure you of that."
Officials intended to report the tests later in an annual report, Clifford said.
These 9,200 cases were different because brain tissue samples were preserved with formalin, which makes them suitable for only one type of test--immunohistochemistry, or IHC.
In the Texas case, officials had declared the cow free of disease in November after an IHC test came back negative. The department's inspector general ordered an additional kind of test, which confirmed the animal was infected.
Veterinarians in remote locations have used the preservative on tissue to keep it from degrading on its way to the department's laboratory in Ames, Iowa. Officials this year asked veterinarians to stop using preservative and send fresh or chilled samples within 48 hours.
The department recently investigated a possible case of BSE that turned up in a preserved sample. Further testing ruled out the disease two weeks ago.
Scientists used two additional tests--rapid screening and Western blot--to help detect BSE in the country's second confirmed case, in a Texas cow in June. They used IHC and Western blot to confirm the first case, in a Washington state cow in December 2003.
"The IHC test is still an excellent test," Clifford said. "These are not simple tests, either."
Clifford pointed out that scientists reran the IHC several times and got conflicting results. That happened, too, with the Western blot test. Both tests are accepted by international animal health officials.
""These 9,200 cases were different because brain tissue samples were preserved with formalin, which makes them suitable for only one type of test--immunohistochemistry, or IHC."
THIS WAS DONE FOR A REASON!
THE IHC test has been proven to be the LEAST LIKELY to detect BSE/TSE in the bovine, and these were probably from the most high risk cattle pool, the ones the USDA et al, SHOULD have been testing. ...TSS
We have to be careful that we don't get so set in the way we do things that we forget to look for different emerging variations of disease. We've gotten away from collecting the whole brain in our systems. We're using the brain stem and we're looking in only one area. In Norway, they were doing a project and looking at cases of Scrapie, and they found this where they did not find lesions or PRP in the area of the obex. They found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had to go back and change the procedure for looking at Scrapie samples. In the USDA, we had routinely looked at all the sections of the brain, and then we got away from it. They've recently gone back. Dr. Keller: Tissues are routinely tested, based on which tissue provides an 'official' test result as recognized by APHIS.
Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't they still asking for the brain? But even on the slaughter, they're looking only at the brainstem. We may be missing certain things if we confine ourselves to one area.
Dr. Detwiler: It seems a good idea, but I'm not aware of it. Another important thing to get across to the public is that the negatives do not guarantee absence of infectivity. The animal could be early in the disease and the incubation period. Even sample collection is so important. If you're not collecting the right area of the brain in sheep, or if collecting lymphoreticular tissue, and you don't get a good biopsy, you could miss the area with the PRP in it and come up with a negative test. There's a new, unusual form of Scrapie that's been detected in Norway. We have to be careful that we don't get so set in the way we do things that we forget to look for different emerging variations of disease. We've gotten away from collecting the whole brain in our systems. We're using the brain stem and we're looking in only one area. In Norway, they were doing a project and looking at cases of Scrapie, and they found this where they did not find lesions or PRP in the area of the obex. They found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had to go back and change the procedure for looking at Scrapie samples. In the USDA, we had routinely looked at all the sections of the brain, and then we got away from it. They've recently gone back.
Dr. Keller: Tissues are routinely tested, based on which tissue provides an 'official' test result as recognized by APHIS .
Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't they still asking for the brain? But even on the slaughter, they're looking only at the brainstem. We may be missing certain things if we confine ourselves to one area.
Completely Edited Version PRION ROUNDTABLE
Accomplished this day, Wednesday, December 11, 2003, Denver, Colorado
CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006
The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade.
The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old.
These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen.
"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."
Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.
USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.
"Everything they did on the Texas cow makes everything USDA did before 2005 suspect," Brown said. ...snip...end
CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...
In this context, a word is in order about the US testing program. After the discovery of the first (imported) cow in 2003, the magnitude of testing was much increased, reaching a level of >400,000 tests in 2005 (Figure 4). Neither of the 2 more recently indigenously infected older animals with nonspecific clinical features would have been detected without such testing, and neither would have been identified as atypical without confirmatory Western blots. Despite these facts, surveillance has now been decimated to 40,000 annual tests (USDA news release no. 0255.06, July 20, 2006) and invites the accusation that the United States will never know the true status of its involvement with BSE.
In short, a great deal of further work will need to be done before the phenotypic features and prevalence of atypical BSE are understood. More than a single strain may have been present from the beginning of the epidemic, but this possibility has been overlooked by virtue of the absence of widespread Western blot confirmatory testing of positive screening test results; or these new phenotypes may be found, at least in part, to result from infections at an older age by a typical BSE agent, rather than neonatal infections with new "strains" of BSE. Neither alternative has yet been investigated.
In June 2005, an inconclusive bovine spongiform encephalopathy (BSE) sample from November 2004, that had originally been classified as negative on the immunohistochemistry test, was confirmed positive on SAF immunoblot (Western blot). The U.S. Department of Agriculture (USDA) identified the herd of origin for the index cow in Texas; that identification was confirmed by DNA analysis. USDA, in close cooperation with the Texas Animal Health Commission (TAHC), established an incident command post (ICP) and began response activities according to USDA’s BSE Response Plan of September 2004. Response personnel removed at-risk cattle and cattle of interest (COI) from the index herd, euthanized them, and tested them for BSE; all were negative. USDA and the State extensively traced all at-risk cattle and COI that left the index herd. The majority of these animals entered rendering and/or slaughter channels well before the investigation began. USDA’s response to the Texas finding was thorough and effective.
Friday, August 29, 2008
CREEKSTONE VS USDA COURT OF APPEALS, BUSH SAYS, NO WAY, NO HOW
see full text of this ongoing cover-up of mad cow disease in the USA. ...
Usda Certified Deadstock Downer Cow School Lunch Program Update
Wednesday, December 10, 2008
Evaluation of FSIS Management Controls Over Pre-Slaughter Activities (Audit Report 24601-7-KC)
Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME. Since previous incidences of TME were associated with common or shared feeding practices, we obtained a careful history of feed ingredients used over the past 12-18 months. ***The rancher was a "dead stock" feeder using mostly (>95%) downer or dead dairy cattle and a few horses. Sheep had never been fed.***
Epidemiology Epidemiologic studies suggest that animals contract the disease by external exposure to the infectious agent, such as by eating contaminated feed. No evidence suggests that the TME agent spreads by contact between unrelated mink or from mother to nursing young. The disease has been identified in both genders and all color phases in animals greater than 1 year old. The first documented TME outbreak in the United States occurred in 1947 on one ranch in Wisconsin and then on a ranch in Minnesota that had received mink from the Wisconsin ranch. In 1961, TME outbreaks occurred on five ranches in Wisconsin. In Factsheet Veterinary Services February 2002 APHIS 1963, outbreaks occurred in Idaho, Minnesota, and Wisconsin. Epidemiologic data from the Minnesota and Wisconsin outbreaks trace the cases in those States to one common purchased food source.
The 1985 Stetsonville Outbreak The most recent TME outbreak occurred on one mink ranch in Stetsonville, WI, in 1985. In the herd of 7,300 adult mink, 60 percent of the animals died. Clinical signs included tail arching, incoordination, and hyperexcitability. At the most advanced stages of the disease, the animals were in trancelike states and eventually died. The outbreak lasted 5 months. Microscopic examination of sections of the brain confirmed the spongelike changes characteristic of TME. Diagnostic tests identified the prion protein. The following year, mink born during the outbreak showed no signs of TME. The late Richard Marsh, a veterinary virologist at the University of Wisconsin who studied the transmission of TME and other TSE's, investigated this outbreak. Marsh learned that the mink were fed a diet composed of fresh meat products from "downer cattle" and commercial sources of fish, poultry, and cereal. Downer cattle are nonambulatory and cannot rise because they are affected with a condition such as a metabolic disease, broken limbs, or a central nervous system disorder. Marsh theorized that the meat from these downer cattle introduced a TSE agent to the mink in which TME resulted. Although Marsh's hypothesis is based on speculation and anecdotal evidence, in 1993 APHIS adjusted its national BSE surveillance program to include testing downer cattle for evidence of a TSE. The brains of more than 20,141 cattle have been examined at APHIS' National Veterinary Services Laboratories and other State diagnostic laboratories. Not a single tissue sample has revealed evidence of BSE or another TSE in cattle.
AND as everyone knows, the rest is history, those dead-stock downers, the most high risk cattle, were NOT tested, and in FACT, was a major source of YOUR CHILDRENS SCHOOL LUNCH PROGRAM, all across the Nation. sorry, these are the most high risk cattle for TSE aka mad cow disease, and i am a bit touchy about this topic. ...sorry. ...terry
DOWNER COW SCHOOL LUNCH PROGRAM
IN CONFIDENCE PERCEPTION OF UNCONVENTENTIONAL SLOW VIRUS DISEASES OF ANIMALS IN THE USA 1985
The Stetsonville outbreak (farmer's name: Brecke). In addition to the downer cows and horses Brecke's mink recieved a cereal supplement. Hartsough's view was that this would contain bone meal and would be from a commercial source. If this were so and it was contaminated with a TME agent why were no other ranches affected? Many mink ranches now feed a commerical pelleted diet.
Brecke was equipped to process LARGE CARCASSES USING A CRUSHER/MIXER WHICH COULD ACCOMMODATE A WHOLE COW!
Wilbur Clarke (reference the Mission, Texas scrapie transmission transmission to cattle study) is now the State Veterinarian for Montana based at Helena. I was given confidential access to sections from the Clarke scrapie-cattle transmission experiment. Details of the experimental design were as supplied previously by Dr. Wrathall (copy of relevant information appended). Only 3 animals (2 inoculated with 2nd pass Suffolk scrapie and 1 inoculated with Angora goat passaged scrapie) showed clinical signs. Clinical signs were characterised by weakness, ''a stilted hindlimb gait'', disorientation, ataxia and, terminally, lateral recumbency. The two cattle from which I examined material were inocluated at 8 months of age and developed signs 36 months pi (goat scrapie inoculum) and 49 months pi (one of the Suffolk scrapie inoculated) respectively. This latter animal was killed at 58 months of age and so the clinical duration was only 1 month. The neuropathology was somewhat different from BSE or the Stetsonville TME in cattle. Vacuolar changes were minimal, to the extent that detection REQUIRED CAREFUL SEARCHING. Conversely astrocyte hypertrophy was a widespread and prominent feature. The material requires DETAILED NEUROPATHOLOGICAL ASSESSMENT BUT WHETHER OR NOT THIS WILL BE DONE REMAINS A QUESTION.
were there extensive neurologic lesions, which are primary for BSE, such as severe vacuolation of neurons and neuropil or neuronal necrosis and gliosis. Although some vacuolation of neuropil, chromotolysis in neurons, and gliosis were seen in the brains of some affected calves, these were industinguishable from those of controls. Vacuolated neurons in the red nucleus of both challenged and normal calves were considered normal for the bovines as previously described (50). PrP-res was found in ALL CHALLENGED CALVES REGARDLESS OF CLINCIAL SIGNS, and the amount of PrP-res positively related to the length of the incubation. ...
WE also conclude from these studies that scrapie in cattle MIGHT NOT BE RECOGNIZED BY ROUTINE HISTOPATHOLOGICAL EXAMINATION OF THE BRAIN AND SUGGEST THAT DETECTION OF PrP-res by immunohistochemistry or immunoblotting is necessary to make a definitive diagnosis. THUS, undiagnosed scrapie infection could contribute to the ''DOWNER-COW'' syndrome and could be responsible for some outbreaks of transmissible mink encephalopathy proposed by Burger and Hartsough (8) and Marsh and harsough (52). ...
Multiple sources of sheep affected with scrapie and two breeds of cattle from several sources were used inthe current study in an effort to avoid a single strain of either agent or host. Preliminary results from mouse inoculations indicate multiple strains of the agent were present in the pooled inoculum (unpublished data). ...
Transmission of the sheep scrapie to cattle was attempted in 1979 by using intracerebral, intramuscular, subcutaneous, and oral routes of inoculation of 5, 8- to 11-month old cattlw with a homologous mixture of brain from 1 affected sheep (61, 62). ONE of the 5 cattle develped neurologic signs 48 months after inoculation. Signs were disorientation, incoordination, a stiff-legged stilted gait, progressive difficulty in rising, and finally in terminal recumbency. The clinical course was 2.5 months. TWO of the 5 cattle similarly inoculated with brain tissue from a goat with scrapie exhibited similar signs 27 and 36 months after incoluation. Clinical courses were 43 an 44 days. Brain lesions of mild gliosis and vacuolation and mouse inoculation data were insufficient to confirm a diagnosis of scrapie. This work remained controversial until recent examination of the brains detected PrP-res in all 3 cattle with neurologic disease but in none of the unaffected cattle (62). Results of these studies are similar to ours and underscore the necessity of methods other than histopathology to diagnose scrapie infection in cattle. We believe that immunologic techniques for detecting PrP-res currently provide the most sensitive and reliable way to make a definitive diagnosis...
Visit to USA ... info on BSE and Scrapie
Saturday, February 21, 2009
Renderers say industry not prepared for FDA feed ban rule ??? WHAT, IT'S 2009 FOR PETE'S SAKE $$$
Two recent articles caught my eye ;
Renderers say industry not prepared for FDA feed ban rule
Food Chemical News
February 2, 2009
BSE, rendering relate to human safety
Emma Struve 02/17/2009
OIE amending the Annex to Decision 2007/453/EC establishing the BSE status of Member States or third countries or regions thereof according to their BSE risk
Saturday, January 24, 2009
Bovine Spongiform Encephalopathy h-BSE ATYPICAL USA 2008 Annual Report Research Project: Study of Atypical Bse
Location: Virus and Prion Diseases of Livestock
2008 Annual Report
Sunday, December 28,
2008 MAD COW DISEASE USA DECEMBER 28, 2008 an 8 year review of a failed and flawed policy
A New Prionopathy OR more of the same old BSe and sporadic CJD
Communicated by: Terry S. Singeltary Sr.
[In submitting these data, Terry S. Singeltary Sr. draws attention to the steady increase in the "type unknown" category, which, according to their definition, comprises cases in which vCJD could be excluded. The total of 26 cases for the current year (2007) is disturbing, possibly symptomatic of the circulation of novel agents. Characterization of these agents should be given a high priority. - Mod.CP]
There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.
He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.
sporadic Fatal Familial Insomnia
JOURNAL OF NEUROLOGY
MARCH 26, 2003
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob
disease in the United States
Email Terry S. Singeltary:
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al  have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?
THE PATHOLOGICAL PROTEIN
Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9
BY Philip Yam
CHAPTER 14 LAYING ODDS
Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.
Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. FREE FULL TEXT
2 January 2000 British Medical Journal U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well
15 November 1999 British Medical Journal vCJD in the USA * BSE in U.S.
Creutzfeldt Jakob Disease
USA PRION UNIT BLOG
Sunday, April 20, 2008 Progress Report from the National Prion Disease Pathology Surveillance Center April 3, 2008
Atypical forms of BSE have emerged which, although rare, appear to be more virulent than the classical BSE that causes vCJD.
see full text ;
CJD TEXAS (cjd clusters)
USA WRITTEN CJD QUESTIONNAIRE ???
The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.
Attending Dr.: Date / Time Admitted : 12/14/97 1228
UTMB University of Texas Medical Branch Galveston, Texas 77555-0543 (409) 772-1238 Fax (409) 772-5683 Pathology Report
FINAL AUTOPSY DIAGNOSIS Autopsy' Office (409)772-2858
FINAL AUTOPSY DIAGNOSIS
I. Brain: Creutzfeldt-Jakob disease, Heidenhain variant.
Thursday, December 04, 2008 2:37 PM
"we have found that H-BSE can infect humans."
personal communication with Professor Kong. ...TSS
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518